Study on the promotion of bacterial biofilm formation by a Salmonella conjugative plasmid and the underlying mechanism.

Abstract

To investigate the effect of the pRST98 plasmid, originally isolated from Salmonella enterica serovar Typhi (S. Typhi), on biofilm (BF) formation, we carried out in vitro experiments using S. Typhi, Salmonella enterica serovar Typhimurium (S. Typhimurium) and Escherichia coli (E. coli). We further explored the effects of pRST98 in vivo by establishing two animal models, a tumor-bearing mouse model and a mouse urethral catheter model. Moreover, we examined the relationship between the quorum-sensing (QS) system and pRST98-mediated BF formation. These studies showed that pRST98 enhanced BF formation in different bacteria in vitro. In both animal models, pRST98 promoted BF formation and caused more severe pathological changes. It was previously reported that Salmonella senses exogenous N-acylhomoserine lactones (AHLs) through the regulatory protein SdiA and regulates the expression of genes including the virulence gene rck, which is located on the virulence plasmid of some serotypes of Salmonella. In this study, we confirmed the locus of the rck gene on pRST98 and found that AHLs increased rck expression in pRST98-carrying strains, thereby enhancing bacterial adherence, serum resistance and bacterial BF formation. In conclusion, the Salmonella conjugative plasmid pRST98 promotes bacterial BF formation both in vitro and in vivo, and the mechanism may relate to the AHL-SdiA-Rck signaling pathway.